Seed vigor affects seed germination and seedling emergence, and therefore is an important agronomic trait in rice. Small auxin-up RNAs (SAURs) function in a range of developmental processes, but their role in seed vigor remains unclear. Here, we observed that disruption of OsSAUR33 resulted in reduced germination rates and low seed uniformity in early germination. Expression of OsSAUR33 was higher in mature grains and early germinating seeds. RNA-seq analysis revealed that OsSAUR33 modulated seed vigor by affecting the mobilization of stored reserves during germination. Disruption of OsSAUR33 increased the soluble sugar content in dry mature grains and seeds during early germination. OsSAUR33 interacted with the sucrose non-fermenting-1-related protein kinase OsSnRK1A, a regulator of the sugar signaling pathway, which influences the expression of sugar signaling-related genes during germination. Disruption of OsSAUR33 increased sugar-sensitive phenotypes in early germination, suggesting OsSAUR33 likely affects seed vigor through the sugar pathway. One elite haplotype of OsSAUR33 associated with higher seed vigor was identified mainly in indica accessions. This study provides insight into the effects of OsSAUR33 on seed vigor in rice.The effect of grazing on leaf photosynthesis has been extensively studied. However, the influence of grazing on photosynthesis in other green tissues, especially spike, has remained poorly understood. This study investigated the impact of different grazing intensities (light grazing (LG), medium grazing (MG), and heavy grazing (HG)) on leaf and spike photosynthesis parameters and photosynthetic pigments of three grass species (Stipa purpurea, Achnatherum inebrians, and Leymus secalinus) on an alpine steppe in the Qilian Mountains. Grazing promoted leaf photosynthesis rate in S. purpurea and L. secalinus but reduced it in A. inebrians. Conversely, spike photosynthesis rate decreased in S. purpurea and L. secalinus under intense grazing, while there was no significant difference in spike photosynthesis rate in A. inebrians. The leaf and spike net photosynthetic rate (Pn) and transpiration rate (Tr) in S. purpurea were the greatest among the three species, while their organ temperatures were the lowest. On the other hand, grazing stimulated leaf chlorophyll biosynthesis in S. purpurea and L. secalinus but accelerated leaf chlorophyll degradation in A. inebrians. Furthermore, spike chlorophyll biosynthesis was inhibited in the three species under grazing, and only L. secalinus had the ability to recover from the impairment. Grazing had a positive effect on leaf photosynthesis parameters of S. purpurea and L. secalinus but a negative effect on those of A. inebrians. However, spike photosynthesis parameters were negatively influenced by grazing. Among the three species investigated, S. purpurea displayed the greatest ability for leaf and spike photosynthesis to withstand and acclimate to grazing stress. This study suggests that moderate grazing enhanced leaf photosynthetic capacity of S. purpurea and L. secalinus but reduced it in A. inebrians. However, spike photosynthetic capacity of three grass species decreased in response to grazing intensities.Converting crystalline compounds into co-amorphous systems is an effective way to improve the solubility of poorly water-soluble drugs. It is, however, of critical importance for the physical stability of co-amorphous systems to find the optimal mixing ratio of the drug with the co-former. In this study, a novel approach for this challenge is presented, exemplified with the co-amorphous system carvedilol-tryptophan (CAR-TRP). Following X-ray powder diffraction (XRPD) and differential scanning calorimetry (DSC) of the ball-milled samples to confirm their amorphous form, Fourier-transform infrared spectroscopy (FTIR) and principal component analysis (PCA) were applied to investigate intermolecular interactions. A clear deviation from a purely additive spectrum of CAR and TRP was visualized in the PCA score plot, with a maximum at around 30% drug (mol/mol). This deviation was attributed to hydrogen bonds of CAR with TRP ether groups. The sample containing 30% drug (mol/mol) was also the most stable sample during a stability test. Using the combination of FTIR with PCA is an effective approach to investigate the optimal mixing ratio of non-strong interacting co-amorphous systems.The abundant miRNAs in urinary extracellular vesicles (EVs) represent ideal reservoirs for biomarker discovery, especially in renal cell carcinoma (RCC). However, the content and biological functions of microRNAs contained in urinary EVs in RCC remain ambiguous. In this study, urinary EVs were isolated and characterized from RCC patients and healthy volunteers. Differentially expressed microRNAs in urinary EVs were screened by small RNA sequencing. The target gene and biological functions of selected microRNAs were investigated through multifaceted methods. Results indicated that miR-224-5p was significantly upregulated in urinary EVs of RCC patients compared to healthy volunteers. The overexpression of miR-224-5p inhibited RCC cell proliferation and induced cell cycle arrest. The gene CCND1 encoding cyclin D1 was identified as a direct target of miR-224-5p via prediction and validation. Moreover, the invasive and metastatic abilities of RCC cells were enhanced by miR-224-5p. Interestingly, miR-224-5p also increased the stability of PD-L1 protein by inhibiting CCND1. This effect could be transmitted via EVs and further promoted the resistance of RCC cells to T cell-dependent toxicity. In summary, urinary EVs containing miR-224-5p were identified as a potential biomarker in RCC. Regulation of PD-L1 protein expression by miR-224-5p through suppressing CCND1 elucidates new roles of miR-224-5p in RCC progression.Arrestins are a small family of four proteins in most vertebrates that bind hundreds of different G protein-coupled receptors (GPCRs). https://www.selleckchem.com/products/ala-gln.html Arrestin binding to a GPCR has at least three functions precluding further receptor coupling to G proteins, facilitating receptor internalization, and initiating distinct arrestin-mediated signaling. The molecular mechanism of arrestin-GPCR interactions has been extensively studied and discussed from the "arrestin perspective", focusing on the roles of arrestin elements in receptor binding. Here, we discuss this phenomenon from the "receptor perspective", focusing on the receptor elements involved in arrestin binding and emphasizing existing gaps in our knowledge that need to be filled. It is vitally important to understand the role of receptor elements in arrestin activation and how the interaction of each of these elements with arrestin contributes to the latter's transition to the high-affinity binding state. A more precise knowledge of the molecular mechanisms of arrestin activation is needed to enable the construction of arrestin mutants with desired functional characteristics.